The undigested high-molecular-weight fraction (HMF) of soybean protein prepared after exhaustive digestion by microbial proteases significantly decreased serum cholesterol levels to approximately 45% (p less than 0.05) of those observed with the parent protein in rats fed diets containing cholesterol (0.5%) and sodium cholate (0.125%). HMF bound conjugated bile salts in vitro and significantly increased fecal excretion of both neutral and acidic steroids by 65-95% and 80-170% more, respectively (p less than 0.05), than did the intact protein. Extraction of HMF with methanol slightly decreased the activity, but the methanol-soluble fraction was not regarded as a principal determinant. Soybean saponin at the dietary level equivalent to that contained in HMF did not effectively lower serum cholesterol. The activity was not necessarily duplicated even when methanol-treated fractions were recombined. Further degradation of the methanol-extracted HMF by various proteases resulted in loss of activity. HMF obtained after pepsin digestion exerted a potential similar to that of HMF prepared after digestion by microbial proteases.

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The antibacterial activity of the polymyxin group against gram-negative bacteria has been explained as owing to increased permeability of the cell envelope consisting of cell wall and cytoplasmic membrane and the resultant leakage of the cell contents (7). Consequently, morphological studies should contribute much to the elucidation of the mechanism of action of these agents (2). We have made detailed observations

Retinoic acid (RA) treatment of SMS ± KCNR neuroblastoma (NB) cells leads to G1 growth arrest and neuronal di erentiation. To investigate the molecular mechanisms by which RA alters cell growth, we analysed the expression and activity of components of the cell cycle machinery after culture in RA. Within 2 days of RA treatment and prior to the arrest of NB cells in the G1 phase of the cell cycle, there is a complete downregulation of G1 cyclin/Cdk activities. Protein levels for the G1 cyclin/Cdks were essentially unchanged during this time although there was a decrease in the steady-state levels of p67 N-Myc and hyperphosphorylated Rb proteins. The Cdk inhibitors, p21 Cip1 and p27 Kip1 were constitutively expressed in KCNR while p15 INK4B and p16 INK4A were not detected. RA induced an increase in the expression of p27 Kip1 but not p21 Cip1 . Furthermore, coincident with the decrease in kinase activity there was an increase in G1 cyclin/Cdk bound p27 Kip1 . These results indicate that changes in the level of p27 Kip1 and its binding to G1 cyclin/Cdks may play a key role in RA induced growth arrest of NB cells.

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